銅は,特定のDNA結合タンパク質の形状を変更することによって,メタロチオネインの遺伝子転写を活性化します
1Laboratory of Biochemistry, National Cancer Institute, Bethesda, Maryland 20892.
Cell
|November 18, 1988
まとめ
酵母における銅のホメオスタシスは,銅が存在する場合にのみDNAを結合する規制タンパク質に依存しています. 銅の結合は,形状の変化を誘導し,遺伝子転写を活性化し,新しい銅のクラスターモデルを明らかにします.
科学分野:
- 分子生物学は分子生物学である.
- バイオケミストリー バイオケミストリー
- イースト遺伝学 イースト遺伝学
背景:
- 銅のホメオスタシスは,細胞の機能に不可欠です.
- メタロチオニンと調節タンパク質は,酵母銅調節の重要な役割を果たしています.
- 調節タンパク質はメタロチオネインの遺伝子転写を制御する.
研究 の 目的:
- 酵母における銅誘発遺伝子調節のメカニズムを調査する.
- 調節タンパク質の機能領域を特定する.
- 銅結合とDNA相互作用の構造的基礎を解明する.
主な方法:
- DNA結合測定は,銅の存在と不在で行われます.
- 機能ドメインをマッピングするための部分タンパク質分解.
- インビトロとインビボの転写アッセイ.
- 構造分析とモデリング.
主要な成果:
- 調節タンパク質は,銅の存在下でメタロチオネインの遺伝子配列を特定して結合する.
- DNA結合機能と銅感知機能の両方がアミノターミナル領域にあります.
- 銅は,DNA結合領域における重要な構成変化を誘導する.
- シルバーイオンはまた,DNA結合ドメインを活性化し,遺伝子転写を誘導します.
結論:
- DNA結合ドメインのための新しい銅クラスターモデルが提案されています.
- 調節タンパク質のメカニズムは,銅媒介による形状の変化を含む.
- DNA結合ドメインとmetallothionein.in.の間に構造的な類似性が存在する.
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